Evidence map›Paper›PMID 22023617›Full record

ArticleCurrent neurovascular research2011

Erythropoietin and Wnt1 govern pathways of mTOR, Apaf-1, and XIAP in inflammatory microglia.

Yan Chen Shang, Zhao Zhong Chong, Shaohui Wang, Kenneth Maiese

Abstract read
In one paragraph

Article in Current neurovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
4.7field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

68 citing papers in PubMed, 93 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Cognitive Impairment in Multiple Sclerosis.Bioengineering (Basel, Switzerland) · 2023
    Review
  5. Review
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Alzheimer's Disease and Protein Kinases.Advances in experimental medicine and biology · 2021
    Article
  17. Article
  18. Research in pharmaceutical sciences · 2020
    Article
  19. New Insights for nicotinamide: Metabolic disease, autophagy, and mTOR.Frontiers in bioscience (Landmark edition) · 2020
    Review
  20. Review

8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Yan Chen ShangLaboratory of Cellular and Molecular Signaling, University of Medicine and Dentistry, New Jersey Medical School, Newark, New Jersey 07101, USA.
Zhao Zhong Chong
Shaohui Wang
Kenneth Maiese
Rutgers, The State University of New Jersey · US

Funding

RESEARCH CORE-- SIGNAL TRANSDUCTIONP30ES006639 · NIEHS · WAYNE STATE UNIVERSITY · PI RUNGE-MORRIS, MELISSA A · 1994 to 2008
$13.1M
Impacting Oxidative Stress and Cell Injury through Novel Pathways of the Wnt GeneR01NS053946 · NINDS · WAYNE STATE UNIVERSITY · PI MAIESE, KENNETH · 2007 to 2011
$2.4M
NIEHS NIH HHS P30 ES006639NIEHS NIH HHS P30 ES06639NINDS NIH HHS R01 NS053946
6 · The paper itself

Abstract

Inflammatory microglia modulate a host of cellular processes in the central nervous system that include neuronal survival, metabolic fluxes, foreign body exclusion, and cellular regeneration. Elucidation of the pathways that oversee microglial survival and integrity may offer new avenues for the treatment of neurodegenerative disorders. Here we demonstrate that erythropoietin (EPO), an emerging strategy for immune system modulation, prevents microglial early and late apoptotic injury during oxidant stress through Wnt1, a cysteine-rich glycosylated protein that modulates cellular development and survival. Loss of Wnt1 through blockade of Wnt1 signaling or through the gene silencing of Wnt1 eliminates the protective capacity of EPO. Furthermore, endogenous Wnt1 in microglia is vital to preserve microglial survival since loss of Wnt1 alone increases microglial injury during oxidative stress. Cellular protection by EPO and Wnt1 intersects at the level of protein kinase B (Akt1), the mammalian target of rapamycin (mTOR), and p70S6K, which are necessary to foster cytoprotection for microglia. Downstream from these pathways, EPO and Wnt1 control "anti-apoptotic" pathways of microglia through the modulation of mitochondrial membrane permeability, the release of cytochrome c, and the expression of apoptotic protease activating factor-1 (Apaf-1) and X-linked inhibitor of apoptosis protein (XIAP). These studies offer new insights for the development of innovative therapeutic strategies for neurodegenerative disorders that focus upon inflammatory microglia and novel signal transduction pathways.

Indexed as

Analysis of VarianceAnimalsAntibodiesApoptotic Protease-Activating Factor 1Cell DeathCell Line, TransformedCytochromes cDNA FragmentationDose-Response Relationship, DrugErythropoietinGene Expression RegulationGlucoseHumansHypoxiaIn Situ Nick-End LabelingMembrane Potential, MitochondrialAntibodiesApaf1 protein, mouseApoptotic Protease-Activating Factor 1Cytochromes cErythropoietinGlucosePhosphatidylserinesTOR Serine-Threonine KinasesWnt1 ProteinX-Linked Inhibitor of Apoptosis Protein

Identifiers

PMID22023617
PMCPMC3254854
OpenAlexW2114694618

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.